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亲嗜性病毒整合位点1 ( ecotropic viral integration site 1 , EVI1 )基因高表达与急性髓系白血病( acute myeloid leukemia , AML )的发生、治疗及预后密切相关.已证实 EVI1 能够引起髓系分化和凋亡受阻,且在治疗过程中对化疗药物不敏感,其诱导缓解率和长期生存率低,是 AML 预后不良的分子生物学标记.但其中许多机制仍在探索中,且临床治疗效果欠佳.因此进一步阐明 EVI1 基因介导白血病发生的重要机制以及和 AML 的关系,将为开发新的靶向治疗提供依据.本文就 EVI1 基因表达在急性髓系白血病中的研究进展作一综述.“,”The high expression of ecotropic viral integration site 1 ( EVI1 ) gene is closely related to the occurrence , treatment and prognosis of acute myeloid leukemia ( AML ) . EVI1 is known to cause myeloid differentiation and apoptosis blockade , and is insensitive to chemotherapeutic drugs in the course of treatment . Its induction remission rate and long-term survival rate are low . EVI1 is a molecular biological marker for poor prognosis of AML . However , many of these mechanisms are still being explored , and the clinical treatment is not effective . Therefore , further elucidation of the important mechanism of EVI1 gene-mediated leukemia and its relationship with AML will provide a basis for the development of new targeted therapies . This article reviews the progress of EVI1 gene expression in acute myeloid leukemia .